Inhibition of Notch-1 pathway is involved in rottlerin-induced tumor suppressive function in nasopharyngeal carcinoma cells
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Yingying Hou1,*, Shaoyan Feng2,*, Lixia Wang1, Zhe Zhao1, Jingna Su1, Xuyuan Yin1, Nana Zheng1, Xiuxia Zhou1, Jun Xia3 and Zhiwei Wang1,3,4
1The Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Soochow University, Suzhou, China
2Department of Otolaryngology, Head and Neck Surgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China
3Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui, China
4Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
*These authors have contributed equally to this work
Jun Xia, email: firstname.lastname@example.org
Zhiwei Wang, email: email@example.com
Keywords: rottlerin, nasopharyngeal carcinoma, Notch-1, invasion, apoptosis
Received: March 28, 2017 Accepted: May 24, 2017 Published: July 08, 2017
Recent studies have revealed that rottlerin is a natural chemical drug to exert its anti-cancer activity. However, the molecular mechanisms of rottlerin-induced tumor suppressive function have not been fully elucidated. Notch signaling pathway has been characterized to play a crucial role in tumorigenesis. Therefore, regulation of Notch pathway could be beneficial for the treatment of human cancer. The aims of our current study were to explore whether rottlerin could suppress Notch-1 expression, which leads to inhibition of cell proliferation, migration and invasion in nasopharyngeal carcinoma cells. We performed several approaches, such as CTG, Flow cytometry, scratch healing assay, transwell and Western blotting. Our results showed that rottlerin treatment inhibited cell growth, migration and invasion, and triggered apoptosis, and arrested cell cycle to G1 phase. Moreover, the expression of Notch-1 was obvious decreased in nasopharyngeal carcinoma cells after rottlerin treatment. Importantly, overexpression of Notch-1 promoted cell growth and invasion, whereas down-regulation of Notch-1 inhibited cell growth and invasion in nasopharyngeal carcinoma cells. Notably, we found the over-expression of Notch-1 could abrogate the anti-cancer function induced by rottlerin. Strikingly, our study implied that Notch-1 could be a useful target of rottlerin for the prevention and treatment of human nasopharyngeal carcinoma.
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